Many diseases in humans, including cancers, are caused by genetic errors starting from a single cell. The origin of these genetic errors and the expansion of the abnormal cells carrying these genetic errors are often stochastic processes.
Dr Weini Huang and PhD student Ms Elisa Scanu have developed a general framework to model the dynamics of cancer cells carrying multiple types of extrachromosomal DNA (ecDNA), a genetic error found in more than 30% of tumour samples across various cancer types and correlated to the worst clinical outcomes.
They apply this theoretical framework, based on branching processes, to different biological contexts, where ecDNA copies in the same cell may have distinct oncogenes (species), the same oncogenes but different mutations (genotypes), or different functions without any genetic changes (phenotypes).
Their application in ecDNA species was recently published together with collaborators from the Medical School at Stanford University who specialise in cancer biology. Weini and Elisa analysed the transition probabilities between ecDNA cells with different states. Their theoretical work confirmed that the presence of multiple ecDNA species in cancer cells is not by chance but instead requires additional reproductive advantages for those cells carrying multiple ecDNA species.
The team's work is part of the eDyNAmiC research consortium, which is funded by Cancer Research UK and the National Cancer Institute. This collaboration brings together experts from diverse fields to advance our understanding of cancer and ultimately improve patient outcomes.
The full paper can be accessed on Nature's website.